Acquired immune deficiency syndrome (AIDS) has been known for only a few years as a new infectious disease in man. It is caused by the recently discovered retroviruses HIV 1 and HIV 2, which infect and destroy preferentially CD4.sup.+ T-helper lymphocytes. An immune deficiency is thus produced. This is manifested by the occurrence of opportunistic infections of Kaposi's sarcoma and of so called AIDS-encephalopathy, which are generally progressive and inevitably lead to death. The development of AIDS and the preceding lymphadenopathy syndrome are dependent on active virus replication, which is closely related to the activity of the viral enzyme reverse transcriptase. Therefore effective and selective inhibitors of this polymerase raise the possibility of preventing and slowing the progress of AIDS. The first clinically tested inhibitors of HIV reverse transcriptase, such as Suramin (Germanin.TM.) and HPA 23, have not reached the required level of tolerability of the human body. Only 3'-azido-2,3'-deoxy-thymidine (N.sub.3 -TdR) (German Federal Republic Pat. No. 3,608,606) has shown an unequivocal life extending effect in the case of AIDS patients with pneumocystis carinii pneumoniae, accompanied by improvements in clinical and neurological findings and a temporary restoration of certain immunological functions (Mitsuya et al., Nature 325, 773, 1987). However, the toxic side effects on the bone marrow required blood transfusions in about 50% of the patients treated with it. This indicates that inhibitors of HIV reverse transcriptase with higher selectively and efficacy are required.